AI Article Synopsis

  • - Cell proliferation is vital, but if not properly regulated by the cell cycle and proteins like p16, it can lead to cancer; in many cancers, p16 is found to be inactive, promoting uncontrolled cell division.
  • - The restoration of p16 activity is essential, with strategies like using viral vectors, small molecules, and peptides to suppress abnormal cell growth.
  • - This study aims to enhance the effectiveness of p16 by creating a hybrid peptide that includes a nuclear-localization signal and a short peptide, which targets cancer cell proliferation in chronic myelogenous leukemia by promoting apoptosis.

Article Abstract

Cell proliferation is a crucial step that might promote cancer if deregulated. Therefore, this vital segment is critically controlled by a complicated cell-cycle process in normal cells that is regulated by some regulatory proteins. It has been observed that p16 protein, playing a crucial role in cell-cycle progression/regulation, remains inactivated in different cancer cells. This inactivity of p16 protein leads to the enhancement of cancer cell proliferation by allowing uncontrolled cancer cell division. Hence, the activity of p16 protein needs to be restored using new viral vectors, small molecules as well as peptides to control/suppress this type of abnormal cell proliferation. In this work, we have taken an interesting approach to increase the efficiency and bio-availability of p16 peptide (functional part of p16 protein) to be an aggressive anti-leukemia therapeutic agent by conjugating a nuclear-localized signal (NLS) sequence and a short peptide (AVPI) with it. Moreover, this newly designed NLS attached hybrid peptide greatly affects XIAP expressing but p16 lower expressing human chronic myelogenous leukemia (CML) cell proliferation by targeting both nuclear (CDK4/cyclin D) and cellular factors (XIAP) and promoting the caspase-3 dependent apoptosis pathway.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8864490PMC
http://dx.doi.org/10.1039/d1md00324kDOI Listing

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